Related Experiment Video
Updated: Jun 23, 2025

Noninvasive and Invasive Renal Hypoxia Monitoring in a Porcine Model of Hemorrhagic Shock
Published on: October 28, 2022
Unveiling the heightened susceptibility: Exploring early hypophosphatemia in critically ill trauma patients
Chi-Ju Yang1, Chia-Ming Chang2, Gyu-Ping Chang3
1Department of Pharmacy, National Taiwan University Hospital, Taipei, Taiwan.
Insights
Critically ill trauma patients frequently develop early hypophosphatemia, a condition linked to longer intensive care unit stays. This study highlights the high incidence and potential impact of low phosphate levels in trauma patients.
Area of Science:
- Critical Care Medicine
- Trauma Surgery
- Renal Physiology
Background:
- Phosphorus is essential for physiological functions.
- Hypophosphatemia is common in critically ill trauma patients.
- Early hypophosphatemia may impact patient outcomes.
Purpose of the Study:
- To determine the incidence of early-onset hypophosphatemia in critically ill major trauma patients.
- To explore the relationship between hypophosphatemia and patient outcomes.
- To investigate the role of renal phosphate excretion in trauma-induced hypophosphatemia.
Main Methods:
- Prospective observational study of trauma patients admitted to the ICU.
- Categorization into hypophosphatemia (Hypo-P) and non-hypophosphatemia groups within 72 hours of feeding.
- Assessment of primary outcome: incidence of new-onset hypophosphatemia; secondary outcomes: ICU/hospital stay, ventilation duration, mortality, and urine fractional excretion of phosphate (FEPO4).
Main Results:
- A high incidence of new-onset hypophosphatemia (76.1%) was observed within 72 hours of feeding.
- The Hypo-P group experienced significantly longer ICU stays (8.1 vs. 4.4 days, p=0.0251).
- Elevated urine FEPO4 (29.2% vs. 19.5%, p=0.0242) and trends toward longer hospital stays, ventilation, and mortality were noted in the Hypo-P group.
Conclusions:
- Critically ill trauma patients have a high incidence of early hypophosphatemia, exceeding typical ICU rates.
- Renal phosphate wasting (high urine FEPO4) is a significant factor in early post-trauma phosphate imbalance.
- Hypophosphatemia is associated with prolonged ICU stays, suggesting a need for monitoring and management.
Background:
Phosphorus is a vital mineral crucial for various physiological functions. Critically ill trauma patients frequently experience hypophosphatemia during the immediate post-traumatic phase, potentially impacting outcomes. This study aims to investigate the incidence of early hypophosphatemia in critically major trauma patients.
Methods:
In this prospective observational study, trauma patients admitted to the intensive care unit (ICU) within one day were enrolled. These patients were categorized into Hypo-P groups and Non-hypo groups based on the development of new-onset hypophosphatemia within 72 h after feeding. The primary outcome assessed was the incidence of new-onset hypophosphatemia. The secondary outcomes included ICU and hospital stay, ventilation duration, and mortality.
Results:
76.1% of patients developed a new onset of hypophosphatemia within 72 h after feeding. The Hypo-P group had significantly longer ICU stays (8.1 days ± 5.5 vs. 4.4 days ± 3.1; p = 0.0251) and trends towards extended hospital stay, ventilation duration, and higher mortality. Additionally, they demonstrated significantly higher urine fractional excretion of phosphate (FEPO4) on the first ICU day (29.2% ± 14.23 vs. 19.5% ± 8.39; p = 0.0242).
Conclusion:
Critically ill trauma patients exhibited a significantly higher incidence of early hypophosphatemia than typical ICU rates, indicating their heightened vulnerability. The significantly high urine FEPO4 underscores the crucial role of renal loss in disrupting phosphate metabolism in this early acute phase after trauma. A significant correlation was observed between hypophosphatemia and longer ICU stays. Monitoring and managing phosphate levels may influence outcomes, warranting further investigation.
Related Concept Videos
Acute Pancreatitis II: Clinical Manifestations and Management
Flail Chest-II
Assessment:
1. Clinical Evaluation:
History:

